HoldsUp

The Diary Of A CEO · 2024-08-29 · Steven Bartlett (host), Andrew Huberman

Andrew Huberman: You Must Control Your Dopamine! The Shocking Truth Behind Cold Showers!

52 claims checked against research: 3 contradicted 6 overstated 9 needing context 32 supported 2 unverified

6

Overstated

1:22:55Andrew Hubermanoverstatedmoderate

Deliberate cold exposure causes a large and long-lasting increase in dopamine, epinephrine, and norepinephrine levels.

"What do cold plunges and cold showers do? They stimulate the release of what? The catecholamines, dopamine, epinephrine, norepinephrine, long duration release. That's why it's useful, in my opinion. For all the debate about deliberate cold exposure, does it increase metabolism? Does it not? The answer seems to be probably not much. But it's absolutely clear that it causes a huge increase in adrenaline, dopamine, and norepinephrine that are very long-lasting" (said at 1:22:55)

Human trials of cold water immersion confirm that cold exposure stimulates a substantial increase in plasma norepinephrine (noradrenaline, up to 530%) and dopamine (up to 250%). However, plasma epinephrine (adrenaline) concentrations remain largely unchanged during cold water immersion. Furthermore, the claim that cold exposure does not increase metabolism is inaccurate; human trials show a 350% increase in metabolic rate during 14°C cold water immersion.

1:17:48Andrew Hubermanoverstatedvery low

The depth or severity of the dopamine trough below baseline following a dopamine spike is proportional to the height of the dopamine peak rather than its duration.

"And this trough below baseline, as Anna Lembke taught us with Dopamine Nation, that trough is a state that can last a long time. And it's— HOST: How long? GUEST1: It's proportional to how high that peak in dopamine was. Not how long, but how high that peak in dopamine was." (said at 1:17:48)

The speaker references popular science writing (Anna Lembke's Dopamine Nation, which draws on Solomon and Corbit's classic Opponent-Process Theory of motivation and Koob's neurobiological models of addiction) and asserts as a strict physiological rule that the post-peak dopamine trough is proportional to the peak height rather than its duration. In neurobiology, dopamine signaling operates on multiple distinct temporal and spatial scales (e.g., sub-second phasic transients versus sustained tonic/pharmacological elevations), and homeostatic compensatory changes (such as autoreceptor feedback, vesicle depletion, receptor downregulation, and anti-reward stress systems) are heavily dependent on both the magnitude and the duration/chronicity of exposure. Framing the dopamine trough as strictly proportional to peak height while dismissing duration oversimplifies and misrepresents the complex dynamics of neurochemical homeostasis and opponent processes.

4:49:03Andrew Hubermanoverstatedvery low

Non-sleep deep rest (NSDR) replenishes baseline levels of dopamine in the basal ganglia.

"Replenishes baseline levels of dopamine in the basal ganglia." (said at 4:49:03)

The claim relies on a single small 2002 PET imaging study in eight experienced meditation teachers (PMID: 11958969), which found a 7.9% reduction in [11C]-raclopride binding in the ventral striatum during Yoga Nidra (a form of non-sleep deep rest), indicating an acute ~65% increase in endogenous dopamine release during the practice. However, this study demonstrated transient acute dopamine release during meditation compared to a resting speech-listening control condition, not the restoration or replenishment of depleted baseline dopamine pools over time. Claiming that NSDR replenishes baseline dopamine levels overstates the findings of a small, preliminary acute-phase study.

3:39:18Andrew Hubermanoverstatedmoderate

Studies show an inverse relationship between time spent sitting (such as driving on a hot car seat) and sperm count and viability.

"We know this also from people that sit too much or people that have larger legs. I mean, these studies have actually been done. If you look at the correlation between amount of time seated, especially driving or on a hot car seat, and sperm count and viability, there's kind of an inverse relationship there." (said at 3:39:18)

Studies confirm that prolonged sitting and driving significantly increase scrotal temperature (by 1.5 to 3 °C), and elevated testicular temperature can experimentally impair spermatogenesis. However, epidemiological studies directly examining the relationship between sitting duration (sedentary work or posture) and semen parameters (sperm count, motility, or viability) have generally failed to show a consistent or statistically significant inverse correlation.

3:49:48Andrew Hubermanoverstatedlow

The sexual refractory period is largely caused by an increase in prolactin that suppresses dopamine.

"What I'm saying is that dopamine can overcome the refractory period, but the refractory period itself is largely due to an increase in prolactin that suppresses dopamine." (said at 3:49:48)

While orgasm and ejaculation are followed by a transient surge in prolactin, evidence does not support the claim that the sexual refractory period is largely caused by prolactin suppressing dopamine. Although prolactin release has long been hypothesized to contribute to sexual satiety and modulation of central sexual drive in humans, direct experimental tests refute that acute prolactin elevation is the primary driver of the refractory period. In animal models, pharmacologically blocking or mimicking post-ejaculatory prolactin surges does not shorten or establish the refractory period. Furthermore, drugs like cabergoline that reduce prolactin also act directly as dopamine D2 receptor agonists, confounding whether effects on sexual recovery are due to prolactin reduction or direct dopaminergic stimulation.

3:49:32Andrew Hubermanoverstatedlow

Dopamine can overcome the post-ejaculatory or post-coital refractory period.

"What I'm saying is that dopamine can overcome the refractory period, but the refractory period itself is largely due to an increase in prolactin that suppresses dopamine." (said at 3:49:32)

The statement bundles two related claims. First, evidence from animal models and small human pharmacological trials indicates that dopamine receptor stimulation (or dopamine agonists such as cabergoline or apomorphine) can shorten the post-ejaculatory interval/refractory period. However, the second claim—that the refractory period itself is 'largely due to an increase in prolactin that suppresses dopamine'—is overstated. While an acute prolactin surge is observed following ejaculation in humans and other mammals, experimental studies manipulating prolactin directly (including inhibition or administration of prolactin) have failed to demonstrate that prolactin is the primary causal driver of the post-ejaculatory refractory period, and its exact physiological mechanism remains contested.

Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.